E Prostanoid-1 receptor regulates renal medullary aENaC in rats infused with angiotensin II
Author
dc.contributor.author
González, Alexis A.
Author
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Céspedes, Carlos
es_CL
Author
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Villanueva, Sandra
es_CL
Author
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Michea Acevedo, Luis
es_CL
Author
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Vio, Carlos P.
es_CL
Admission date
dc.date.accessioned
2014-01-07T19:55:28Z
Available date
dc.date.available
2014-01-07T19:55:28Z
Publication date
dc.date.issued
2009
Cita de ítem
dc.identifier.citation
Biochemical and Biophysical Research Communications 389 (2009) 372–377
en_US
Identifier
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0006-291X
Identifier
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https://repositorio.uchile.cl/handle/2250/129105
General note
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Artículo de publicación ISI
en_US
Abstract
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E Prostanoid (EP) receptors play an important role in urinary Na+ excretion. In the kidney, the epithelial
sodium channel (ENaC) is the rate-limiting-step for Na+ reabsorption. We hypothesized that activation of
EP1/EP3 regulates the expression of ENaC in the face of renin–angiotensin–aldosterone-system (RAAS)
activation. In primary cultures of inner medullary collecting duct (IMCD) cells, sulprostone (EP1 > EP3
agonist, 1 lM) and 17 Phenyl trinor (17 Pt, EP1 agonist, 10 lM) prevented the up-regulation of aENaC
mRNA induced by aldosterone (10 nM). In Sprague–Dawley rats infused with angiotensin II (0.4 lg/kg/
min), aENaC expression was up-regulated in renal cortex and medulla coincidently with high plasma
aldosterone levels. Sulprostone and/or 17 Pt prevented this effect in renal medulla but not in cortex.
Immunocytochemistry demonstrated that IMCD cells express EP1. Our results suggest that specific activation
of EP1 receptor during RAAS activation antagonizes the action of aldosterone on aENaC expression
in the renal medulla.
en_US
Patrocinador
dc.description.sponsorship
This work was supported by grants FONDECYT 1080590 and
Programa de Financiamiento Basal PFB 12-2007 (C.P. Vio), FONDECYT
1090223 (L. Michea) and doctoral fellowship from MECESUP
and CONICYT (A.A. Gonzalez).